PLPA 309 student Anna Savage wrote this post (and its sequel). She’s a grad student in Ecology and Evolutionary Biology at Cornell, and studies the frog chytrid.

In the 1970s and ’80s, field biologists studying amphibian populations from around the world started to notice something strange: many of their study populations were disappearing. In some cases, these declines were clearly due to habitat loss and were a direct and obvious result of human activity. However, particularly in Central America and Australia, numerous amphibian populations were disappearing at extremely rapid rates in protected and undisturbed areas, from no obvious environmental cause.

Amphibians are considered “indicator species,” meaning that due to their sensitive skin and requirements for both land and water, they will show signs of environmental stressors or contaminants before other organisms, providing us with an indication that something about the environment has changed. Unexplained amphibian declines are therefore a matter of considerable concern, and the scientific community initially responded by holding the 1989 First World Congress of Herpetology (1, 2), where anecdotal stories of declines and extinctions were shared, and research and global monitoring efforts were initiated. This sparked a considerable body of research, implicating pesticides, herbicides, climate change, and predators in at least some of the known instances of amphibian declines (3-7). However, the most enigmatic declines, where entire populations were disappearing within a single season from protected, pristine land, remained unexplained.

The mystery was solved, or at least the culprit was identified, in 1998 from frogs in Central America and Australia (9). A new species of chytrid fungus, named Batrachochytrium dendrobatidis (Chytridiomycota; Chytridiales), or Bd, was isolated from sick and dead individuals of several frog species and identified as the cause of their decline. The fungus’ culpability was demonstrated by fulfilling Koch’s postulates (8): Bd was isolated from sick frogs, grown in pure culture, used to re-infect other frogs that became ill with the same disease, and then re-isolated from those new individuals (9). Completion of these four steps is the scientific criterion for proving a microorganism causes a disease. However, fulfilling Koch’s postulates did not explain how or why Bd was killing frogs all of the sudden, all over the world. Fungi in the phylum Chytridiomycota are not generally pathogenic; indeed, Bd is the first chytrid fungus identified as a pathogen of vertebrate animals. Further, Bd had never been identified before it began killing frogs, prompting questions about where it came from, and why it had only begun causing disease in amphibian species within the last 30 years.

Eight years have elapsed since Bd was identified as the causal agent of the amphibian disease now referred to as chytridiomycosis. Unfortunately, despite research, monitoring and rehabilitation efforts, the number of species affected by Bd has steadily increased. In 2004, the World Conservation Union (IUCN) published a comprehensive report of global monitoring efforts called the Global Amphibian Assessment (15; I strongly recommend browsing through the IUCN website). Key findings from the assessment are that of the world’s 1,896 known amphibian species, 32% are Red Listed as threatened, 165 species have not been found in years and are presumed to be extinct, 43% have experienced some declines, and another 33% were too rare to even assess. After habitat loss, Bd poses the greatest threat for species extinctions, and has been implicated in declines in Australia, Central America, the United States and Spain (9-14).

In light of these catastrophic findings, it is imperative to fully understand the biology of Bd and the disease pathology of chytridiomycosis. Some characteristics are currently well understood. For example, we know that Bd only infects amphibian tissues containing keratin, which includes the outer skin layers of metamorphosed (adult) individuals, and the mouthparts of tadpoles, which become deformed but do not lead to tadpole mortality (13). The severity of disease is highly dependent on the amount of fungal growth, and frogs with mild infections often show no signs or symptoms, while a high Bd load leads to skin swelling and shedding, redness, lethargy, seizures, and often death. Temperature is the most important environmental factor in determining whether a chytridiomycosis outbreak will occur. Bd grows optimally between 18-24ºC and poorly at 10ºC, but is killed in the laboratory when grown at temperatures above 28ºC (16). Consistent with this finding, most of the species severely affected by chytridiomycosis occur at high elevations in warm climates, where the temperature remains mild year round (10,11). I study a species of leopard frog, Rana yavapaiensis, that is affected by chytridiomycosis in Arizona, USA, but populations that occupy hot springs, where the temperature is consistently above 30ÂºC, never contract chytridiomycosis. Like many chytrid fungi, Bd produces motile asexual spores called zoospores, which propel themselves via a whiplash flagellum “tail” (17). These swimming spores are produced from a monocentric thallus (a single-celled body) that is only 10-30µm wide, and presumably swim through water in search of new amphibian hosts. Consequently, if you have been in a lake or stream where Bd occurs, it is extremely important to decontaminate footwear with bleach to avoid spreading the fungus to new locations.

Research continues to produce new information on chytridiomycosis, but several key aspects remain unknown. First, the precise mechanism by which Bd kills frogs is unclear; none of the compounds produced by Bd cause disease on their own, and fungal cells have never been detected in any tissues other than the outer skin. In addition, we do not understand why amphibian immune systems are unable to fend of Bd infections. Antimicrobial skin peptides produced by dozens of affected frog species have been tested in the lab and effectively kill Bd in a test tube, but this defense mechanism is somehow insufficient in nature. Other aspects of amphibian immunology are poorly understood, but examining frogs with chytridomycosis reveals that they mount very poor immune responses, if any at all. I am currently characterizing several immune system genes in frogs in the hopes of gaining further insight into the pathology of chytridiomycosis.

For more information about chytridiomycosis and amphibian declines, see my next blog entry on how Bd has been spread across the globe, or contact me.

Comments

This is one of the most thorough and articulately written articles I have ever read on Bd. The author possesses a unique blend of solid scientific research with accessible narrative, and is awfully cute if I do say so myself.

Hi, Just a point of clarification. You mention: “…For example, we know that Bd only infects amphibian tissues containing keratin, which includes the outer skin layers of metamorphosed (adult) individuals, and the mouthparts of tadpoles, which become deformed but do not lead to tadpole mortality…”

Tadpole skin (and epithelia in general) contains keratins, what tadpole skin lacks is a keratinized layer of cells, a.k.a. a stratum corneum typical of adult (metamorphosed) skin. As you note, Bd infection does affect certain tissue in the the tadpole’s mouth which is keratinized.

This is one of the best summarized articles I read on chytridiomycosis. Thanks for the information.

About

Most people don't pay much attention to fungi, which include things like mushrooms, molds, yeasts, and mildews. Here at Cornell we think they're pretty fascinating. In fact, even the most disgusting foot diseases and moldy strawberries are dear to our hearts. We'd like to talk to you about fungi, so that like us, you too can tell gross stories at the dinner table. Afterwards, maybe you'll notice some things you would have overlooked before, and we think this could be good for the planet.